Please use this identifier to cite or link to this item: https://doi.org/10.1007/s12017-018-8484-z
Title: Vitamin D3 Supplementation Reduces Subsequent Brain Injury and Inflammation Associated with Ischemic Stroke
Authors: Evans, M.A
Kim, H.A
Ling, Y.H
Uong, S
Vinh, A
De Silva, T.M
Arumugam, T.V 
Clarkson, A.N
Zosky, G.R
Drummond, G.R
Broughton, B.R.S
Sobey, C.G
Keywords: alcohol
calcitriol
interleukin 1beta
interleukin 23p19
interleukin 6
propylene glycol
reduced nicotinamide adenine dinucleotide phosphate oxidase 2
retinoid related orphan receptor gamma
sterile water
transcription factor FOXP3
transforming growth factor beta
autacoid
colecalciferol
cytokine
forkhead transcription factor
Foxp3 protein, mouse
nerve protein
neuroprotective agent
retinoid related orphan receptor gamma
Rorc protein, mouse
animal experiment
animal tissue
antiinflammatory activity
Article
brain infarction size
brain injury
brain ischemia
controlled study
disease association
gamma delta T lymphocyte
immune response
immunocompetent cell
inflammation
lymphocyte count
male
middle cerebral artery occlusion
mouse
neutrophil count
nonhuman
priority journal
protein expression
regulatory T lymphocyte
reperfusion injury
Th17 cell
vitamin supplementation
animal
biosynthesis
brain
C57BL mouse
cerebral artery disease
drug effect
gene expression regulation
genetics
inflammation
macrophage
metabolism
microglia
motor activity
neutrophil chemotaxis
pathology
pathophysiology
T lymphocyte subpopulation
Animals
Brain
Cholecalciferol
Cytokines
Forkhead Transcription Factors
Gene Expression Regulation
Infarction, Middle Cerebral Artery
Inflammation
Inflammation Mediators
Macrophages
Male
Mice, Inbred C57BL
Microglia
Motor Activity
Nerve Tissue Proteins
Neuroprotective Agents
Neutrophil Infiltration
Nuclear Receptor Subfamily 1, Group F, Member 3
T-Lymphocyte Subsets
Issue Date: 2018
Citation: Evans, M.A, Kim, H.A, Ling, Y.H, Uong, S, Vinh, A, De Silva, T.M, Arumugam, T.V, Clarkson, A.N, Zosky, G.R, Drummond, G.R, Broughton, B.R.S, Sobey, C.G (2018). Vitamin D3 Supplementation Reduces Subsequent Brain Injury and Inflammation Associated with Ischemic Stroke. NeuroMolecular Medicine 20 (1) : 147-159. ScholarBank@NUS Repository. https://doi.org/10.1007/s12017-018-8484-z
Rights: Attribution 4.0 International
Abstract: Acute inflammation can exacerbate brain injury after ischemic stroke. Beyond its well-characterized role in calcium metabolism, it is becoming increasingly appreciated that the active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25-VitD3), has potent immunomodulatory properties. Here, we aimed to determine whether 1,25-VitD3 supplementation could reduce subsequent brain injury and associated inflammation after ischemic stroke. Male C57Bl6 mice were randomly assigned to be administered either 1,25-VitD3 (100 ng/kg/day) or vehicle i.p. for 5 day prior to stroke. Stroke was induced via middle cerebral artery occlusion for 1 h followed by 23 h reperfusion. At 24 h post-stroke, we assessed infarct volume, functional deficit, expression of inflammatory mediators and numbers of infiltrating immune cells. Supplementation with 1,25-VitD3 reduced infarct volume by 50% compared to vehicle. Expression of pro-inflammatory mediators IL-6, IL-1β, IL-23a, TGF-β and NADPH oxidase-2 was reduced in brains of mice that received 1,25-VitD3 versus vehicle. Brain expression of the T regulatory cell marker, Foxp3, was higher in mice supplemented with 1,25-VitD3 versus vehicle, while expression of the transcription factor, ROR-γ, was decreased, suggestive of a reduced Th17/γδ T cell response. Immunohistochemistry indicated that similar numbers of neutrophils and T cells were present in the ischemic hemispheres of 1,25-VitD3- and vehicle-supplemented mice. At this early time point, there were also no differences in the impairment of motor function. These data indicate that prior administration of exogenous vitamin D, even to vitamin D-replete mice, can attenuate infarct development and exert acute anti-inflammatory actions in the ischemic and reperfused brain. © 2018, The Author(s).
Source Title: NeuroMolecular Medicine
URI: https://scholarbank.nus.edu.sg/handle/10635/181211
ISSN: 15351084
DOI: 10.1007/s12017-018-8484-z
Rights: Attribution 4.0 International
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